Alcohol-associated liver disease (ALD) is a major contributor to liver-related mortality globally. An increasing body of evidence underscores the pivotal role of platelets throughout the spectrum of liver injury and recovery, offering unique insights into liver homeostasis and pathobiology. Alcoholic-associated steatohepatitis is characterized by the infiltration of hepatic neutrophils. Recent studies have highlighted the extensive distance neutrophils travel through sinusoids to reach the liver injury site, relying on a platelet-paved endothelium for efficient crawling. The adherence of platelets to neutrophils is crucial for accurate migration from circulation to the inflammatory site. A gradual decline in platelet levels leads to diminished neutrophil recruitment. Platelets exhibit the ability to activate neutrophils. Platelet activation is heightened upon the release of platelet granule contents, which synergistically activate neutrophils through their respective receptors. The sequence culminates in the formation of platelet–neutrophil complexes and the release of neutrophil extracellular traps intensifies liver damage, fosters inflammatory immune responses, and triggers hepatotoxic processes. Neutrophil infiltration is a hallmark of alcohol-associated steatohepatitis, and the roles of neutrophils in ALD pathogenesis have been studied extensively, however, the involvement of platelets in ALD has received little attention. The current review consolidates recent findings on the intricate and diverse roles of platelets and neutrophils in liver pathophysiology and in ALD. Potential therapeutic strategies are highlighted, focusing on targeting platelet–neutrophil interactions and activation in ALD. The anticipation is that innovative methods for manipulating platelet and neutrophil functions will open promising avenues for future ALD therapy.

中文翻译：

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酒精相关性肝病中的血小板：与中性粒细胞的相互作用

酒精相关性肝病（ALD）是全球肝脏相关死亡的主要原因。越来越多的证据强调了血小板在整个肝损伤和恢复过程中的关键作用，为肝脏稳态和病理生物学提供了独特的见解。酒精相关性脂肪性肝炎的特征是肝中性粒细胞浸润。最近的研究强调，中性粒细胞通过血窦到达肝损伤部位的距离很远，依靠血小板铺成的内皮细胞进行有效的爬行。血小板与中性粒细胞的粘附对于从循环系统准确迁移到炎症部位至关重要。血小板水平逐渐下降导致中性粒细胞募集减少。血小板表现出激活中性粒细胞的能力。血小板颗粒内容物释放后，血小板活化增强，通过各自的受体协同激活中性粒细胞。该序列最终形成血小板-中性粒细胞复合物，并且中性粒细胞胞外陷阱的释放加剧了肝脏损伤，促进炎症免疫反应，并引发肝毒性过程。中性粒细胞浸润是酒精相关性脂肪性肝炎的一个标志，中性粒细胞在 ALD 发病机制中的作用已被广泛研究，然而，血小板在 ALD 中的参与却很少受到关注。当前的综述整合了关于血小板和中性粒细胞在肝脏病理生理学和 ALD 中复杂而多样的作用的最新发现。强调了潜在的治疗策略，重点关注 ALD 中的血小板-中性粒细胞相互作用和激活。我们预计，控制血小板和中性粒细胞功能的创新方法将为未来 ALD 治疗开辟有希望的途径。